ライフサイエンスコーパス: LDHA

1 LDHA also promoted GH3 cell proliferation through induct

2 okinase 1 (HK1) and lactate dehydrogenase A (LDHA) - both of which regulate the metabolic switch - an

3 Lactate dehydrogenase A (LDHA) catalyzes the conversion of pyruvate to lactate, u

4 lls (HSCs), whereas lactate dehydrogenase A (LDHA) deletion significantly inhibits the function of bo

5 Lactate dehydrogenase A (LDHA) has been reported to be involved in the initiation

6 Here, we show that lactate dehydrogenase A (LDHA) is induced in activated T cells to support aerobic

7 kinase 2 (HK2), and Lactate Dehydrogenase A (LDHA) were each significantly higher in MYCN-amplified n

8 duced activation of lactate dehydrogenase A (LDHA), an enzyme that catalyses the interconversion of p

9 h as those encoding lactate dehydrogenase A (LDHA), solute transporter MCT1, and hexokinase 1 (HK1) -

10 ate lactate through lactate dehydrogenase A (LDHA), which is encoded by a target gene of c-Myc and hy

11 kinase 1 (PDK1) and lactate dehydrogenase A (LDHA).

12 In addition, LDHA knockdown or LDHA Y10F rescue expression in human c

13 ts from regulatory regions of PGK1, ENO1 and LDHA genes.

14 together, these data suggest that HIF1A and LDHA are important targets for hypoxia-driven drug resis

15 Constitutive expression of HK2 and LDHA during differentiation leads to neuronal cell death

16 C, transcriptional activators of the HK2 and LDHA genes, decrease dramatically.

17 onserved canonical E boxes in ENO1, HK2, and LDHA occur in 31- to 111-bp islands with high interspeci

18 iated with a drop in levels of LDHA mRNA and LDHA and hypoxia-inducible factor-1alpha proteins.

19 Additionally, PDK1- and LDHA-overexpressing cells exhibited decreased oxygen con

20 RNA encoding the glycolytic enzymes PFKP and LDHA.

21 sion of the glycolytic genes GLUT1, PKM2 and LDHA, and of CDC25A; thus, Cdc25A upregulates itself in

22 , thereby activating transcription of BNIP3, LDHA, PDK1, and SLC2A1, which encode proteins that are r

23 such as 63 exhibit low nM inhibition of both LDHA and LDHB, submicromolar inhibition of lactate produ

24 in this interval, resulting in the order CEN-LDHA-SAA1-TPH-D11S1310-(D11S1888/KCNC1 )-MYOD1-D11S902D1

25 leic acid or expression of phospho-deficient LDHA Y10F sensitized the cancer cells to anoikis inducti

26 hexokinase (HK2) and lactate dehydrogenase (LDHA) expression, together with a switch in pyruvate kin

27 is an achievable and tolerable treatment for LDHA-dependent tumors.

28 Furthermore, LDHA phosphorylation at Y10 positively correlated with p

29 icantly associated with expression of GLUT1, LDHA, PDK1, LOX, LOXL2, and L1CAM mRNA in human breast c

30 and choline metabolism including GLUT1, HK2, LDHA and CHKA.

31 hydrogenase subunit LDHBx can also co-import LDHA, the other LDH subunit, into peroxisomes.

32 )C MRS of pyruvate to monitor alterations in LDHA activity and expression caused by PI3K pathway inhi

33 Instead, LDHA maintains high concentrations of acetyl-coenzyme A

34 suggesting that Y10 phosphorylation-mediated LDHA activity promotes cancer cell invasion and anoikis

35 ay crystallography to develop small molecule LDHA inhibitors.

36 lation and transcription of Ifng Ablation of LDHA in T cells protects mice from immunopathology trigg

37 Moreover, robust target engagement of LDHA by lead compounds was demonstrated using the cellul

38 ansgenic mice showed decreased expression of LDHA and PDK1 when compared with controls.

39 ple myeloma, and that specific inhibition of LDHA and HIF1A can restore sensitivity to therapeutic ag

40 Accordingly, oxamate-induced inhibition of LDHA suppressed glucose uptake, lactate secretion, invas

41 Hence, inhibition of LDHA with FX11 is an achievable and tolerable treatment

42 Knockdown of LDHA can restore sensitivity of bortezomib resistance ce

43 and were associated with a drop in levels of LDHA mRNA and LDHA and hypoxia-inducible factor-1alpha p

44 udy, we showed that the expression levels of LDHA mRNA and protein were significantly elevated in inv

45 Overexpression of LDHA in a PA cell line (GH3) promoted glucose uptake thr

46 ells, suggesting that Y10 phosphorylation of LDHA may represent a promising therapeutic target and a

47 Here, we report that reduction of LDHA by siRNA or its inhibition by a small-molecule inhi

48 Furthermore, how reduction of LDHA expression by interference or antisense RNA inhibit

49 Previous studies with reduction of LDHA expression indicate that LDHA is involved in tumor

50 However, the potential role of LDHA in pituitary adenoma (PA) remains unknown.

51 udies have focused on the ubiquitous role of LDHA in tumor metabolism and growth, our data reveal tha

52 In addition, LDHA knockdown or LDHA Y10F rescue expression in human cancer cells result

53 Maintenance of PDK1 or LDHA expression in certain regions of the brain may expl

54 e show that overexpression of either PDK1 or LDHA in a rat CNS cell line (B12) confers resistance to

55 In contrast, cells expressing either PDK1 or LDHA maintained a lower mitochondrial membrane potential

56 s inhibited in the absence of either PKM2 or LDHA, indicating that the cell-state-specific responses

57 in multiple myeloma, specifically targeting LDHA, can be beneficial to inhibit tumor growth and over

58 We demonstrate that LDHA is phosphorylated at tyrosine 10 by upstream kinase

59 Our findings demonstrate that LDHA phosphorylation and activation provide pro-invasive

60 Our data indicate that LDHA is involved in promoting the progression of PA, and

61 h reduction of LDHA expression indicate that LDHA is involved in tumor initiation, but its role in tu

62 ctor T cell differentiation and suggest that LDHA may be targeted therapeutically in autoinflammatory

63 These results also suggest that LDHA represents a novel, pharmacologically tractable tar

64 ween a Chk1 inhibitor and chloroquine or the LDHA/LDHB inhibitor GSK 2837808A.

65 henotype in inducing drug resistance through LDHA and HIF1A in multiple myeloma, and that specific in

66 lified neuroblastoma cells are "addicted" to LDHA enzymatic activity, as its depletion completely inh

67 l lines while gain-of-function studies using LDHA or HIF1A induced resistance in bortezomib-sensitive

68 In vivo, LDHA overexpression promoted tumor growth, and oxamate d

69 RPL4, RPL8, RPL18, RPS9, RPS18, TFRC, YWHAZ, LDHA, SDHA).